This work will characterize the cellular inflammatory events that cause the spontaneous regression of syngeneic tumors in animals. Mechanisms which kill or injure tumor cells in vivo will be identified and characterized, thus providing a rational basis for immunologic intervention in the neoplastic process. Our systematic approach first will involve the identification and quantitation of inflammatory cell types that are found in regressing neoplasms. This will be accomplished by demonstrating multiple identifying features of individual cell types in frozen tumor sections and in suspensions obtained from disaggregated neoplasms. Selective depletion of inflammatory cells from intact, tumor-bearing mice then will be used to determine which cell types actually have a functional role in the mediation of tumor regression. Functional importance in the regression process will be confirmed for each cell type by adoptive transfer and homing experiments, as well as by quantitative assays of cytotoxicity in vitro and in vivo. Purified populations of inflammatory cells will be used in these investigations. A wide range of neoplasms will be studied, thus insuring that common pathways involved in the injury of a variety of neoplastic cell types will be identified. Finally, when a clear understanding of the regression process has been obtained, we will compare the cellular mechanisms essential for host defense against neoplasia in mice with regressing and progressing neoplasms. By so doing we will show which cell-mediated, antitumor responses are altered in the face of tumor progression.